The object here is to obtain insight into the genetic control of capsid length in bacteriophage T4 in which mutations are known that cause alteration of capsid length. The most extensively studied set of such mutations is the group of more than 50 ptg mutations that have been mapped to 8 genetic sites distributed in three tight clusters in gene 23 (major capsid structural protein). That these clusters identify 3 short segments of the protein whose interactions play decisive roles in controlling capsid length is suggested not only by the remarkable map distribution of these mutations, but also by the specificity of their suppression by mutations in other genes. We will compare the amino acid sequences of normal and mutant gene 23 proteins, expecting to learn which amino acid substitutions cause loss of fidelity in capsid-length determination. Both DNA and protein sequencing are being employed. Another type of mutation that occurs in gene 23 is known as "bypass-24". It renders dispensable the normally essential gene 24. Such mutations do, in some instances, also cause capsid length modification. Their distribution in gene 23 is also being analyzed, and the assumption of the gene-24 function by gene 23 will be investigated. A third type of mutation that maps in gene 23 is the "bypass-31" type which occurs at at least two sites. Gene-31 plays an essential role for capsid development in wild-type T4. We will attemp to get some indication of how that normal requirement can be circumvented by comparing the alteration of gene-23 protein by these mutations.